Glaucoma in Pseudophakia And Aphakia

Dr. Aishwarya R. Mulay
Published Online: April 1st, 2021 | Read Time: 23 minutes, 7 seconds

Glaucoma in pseudophakia and aphakia is secondary glaucoma in which intraocular pressure (IOP) is elevated following cataract removal. This diagnosis is given only if there was no glaucoma prior to cataract removal.[1] The terms aphakic and pseudophakic glaucoma have been previously used in literature. Currently, this terminology is not preferred. Glaucoma in pseudophakia and aphakia refer to conditions that cause increased intraocular pressure (IOP) soon after surgery as well as to those conditions that occur much later.[2]

Epidemiology :

Depending on the studies, the estimate for the incidence of glaucoma post-cataract surgery varies widely. In patients with aphakia, chronic glaucoma post-cataract surgery was found to be less prevalent at 3% than a transient increase in pressure with varying percentages of pressure rise post-cataract surgery [3]. Other sources report the incidence of 5-41%[4].

In patients with pseudophakia, the incidence of IOP rise went down with an advent of the extracapsular cataract extraction (ECCE) and posterior chamber intraocular lens (PCIOL) implantation. Transient increases in IOP are seen at rates of 29-50% on the first postoperative day in the eyes without pre-existing glaucoma. Chronic glaucoma prevalence in pseudophakic eyes post-surgery was noted between 2.1-4% after the standard extracapsular extraction. Glaucoma was also found in 11.3% of eyes following a secondary anterior chamber extracts[3].

This intraocular pressure elevation occurs in pseudophakic and aphakic eyes as a result of several mechanisms including:[5]

I. Open-angle glaucoma

A. Early-onset (within the first postoperative week) :

1. Pre-existing chronic open-angle glaucoma

2. Chymotrypsin-induced glaucoma

3. Hyphema/debris

4. Viscoelastic material

5. Idiopathic pressure elevation

B. Intermediate onset (after a first postoperative week)

1. Pre-existing chronic open-angle glaucoma

2. Vitreous in the anterior chamber

3. Hyphema

4. Inflammation

5. Lens particle glaucoma

6. Corticosteroid-induced glaucoma

7. Ghost-cell glaucoma

C. Late-onset (more than 2 months postoperatively)

1. Pre-existing chronic open-angle glaucoma

2. Ghost-cell glaucoma

3. Neodymium: yttrium-aluminum-garnet (Nd:YAG) laser capsulotomy

4. Vitreous in the anterior chamber

5. Late-occurring hemorrhage

6. Chronic inflammation

II. Angle-closure glaucoma

A.With pupillary block

1. Anterior hyaloid face

2. Posterior lens capsule

3. Intraocular lens

4. Posterior synechiae

5. Silicone oil

B. Aqueous misdirection (malignant glaucoma)

C. Without pupillary block

1. Pre-existing angle-closure glaucoma

2. Inflammation/hyphema

3. Prolonged anterior chamber shallowing

4. Iris incarceration in cataract incision

5. Intraocular lens haptics

6. Neovascular glaucoma

7. Epithelial ingrowth

8. Fibrous ingrowth

9. Endothelial proliferation

10. The proliferation of iris melanocytes across the trabecular Meshwork

With any cataract procedure, early and late postoperative IOP elevations can occur by a wide variety of mechanisms. The mechanism of the IOP rise appears to be complex and includes the following:

1. Inflammation with the release of active substances, including prostaglandins and the formation of secondary aqueous humor.

2. Watertight wound closure with multiple fine sutures limiting the ‘safety valve’ leak of aqueous humor.

3. Deformation of the limbal area, reducing trabecular outflow.

4. Obstruction of the trabecular meshwork by pigment, blood, lens particles, inflammatory cells, and viscoelastic substances [5]

Glaucoma From Viscoelastic Substances

Viscoelastic substances often are employed in cataract surgery to protect the corneal endothelium and to facilitate intraocular lens (IOL) insertion. Sodium hyaluronate, the agent with perhaps the widest clinical use, frequently causes marked postoperative IOP elevations. The IOP reaches a maximum in 12–16 hours and then abates spontaneously over the next 72 hours.[5] The most likely mechanism of IOP elevation is temporary obstruction of the trabecular meshwork by the viscoelastic.[6]

Inflammation and hemorrhages:

Transient postoperative inflammation occurs to some degree after every cataract extraction. When excessive, obstruction of the trabecular meshwork by inflammatory cells, blood cells, and fibrin may lead to IOP elevations. The inflammatory response and associated glaucoma may be particularly prominent when the lens or cortical fragments are retained in the vitreous or anterior chamber.

Intraocular lens implants especially anterior chamber lenses and iris-supported lenses increase the chances of post-operative uveitis because of the movement of the lens against the iris and the subsequent cellular reaction. Posterior chamber lenses are least likely to induce uveitis. This may be associated with hyphema and glaucoma, which has been referred to as uveitis, glaucoma, and hemorrhage (UGH) syndrome. One cause of late hemorrhage is vascularised wound. Postoperative bleeding from any source may lead to IOP elevation, including ghost cell glaucoma from vitreous hemorrhage.[6]

Pigment Dispersion :

Variable amounts of pigment granules, primarily from the iris pigment epithelium, are dispersed into the anterior chamber with all cataract operations. Excessive pigment dispersion can lead to transiently elevated IOP in aphakic or pseudophakic eyes, with the latter occasionally leading to a chronic form of glaucoma.[6]Pigment dispersion and elevated IOP have been described with posterior chamber IOLs and, in a few cases, with iris fixation lenses. In most instances, the lenses have been decentered, tilted, excessively mobile, too small, or reversed in position, creating excess friction between the optic or haptic and the iris pigment epithelium.

The pigment particles rubbed off the iris accumulate in the trabecular meshwork, where they obstruct aqueous humor outflow in a manner analogous to pigmentary glaucoma. Patients with this entity are responsive to standard medical treatment for glaucoma and to ALT. In some cases, pupillary dilation or constriction may reduce the pigment dispersion. If IOP cannot be controlled, the IOL should be replaced or stabilized.[5]

Vitreous Filling the Anterior Chamber :

Vitreous in the anterior chamber is a rare cause of glaucoma. Glaucoma usually begins within weeks after cataract surgery but may be delayed for months. When examined, these eyes demonstrate elevated IOP and open angles. Vitreous fills the anterior chamber and appears to be in contact with the trabecular meshwork and obstruct the outflow system. In some cases mechanism includes inflammation, pupillary block, and the formation of peripheral anterior synechiae.[5]Some cases resolve on their own, others require a surgical procedure such as iridotomy or anterior vitrectomy and laser vitreolysis.[6]

Pupillary Block

In Aphakia

The pathogenesis of pupillary block in aphakia can be caused by adherence between the iris and anterior vitreous face, which increases the resistance of aqueous humor flow into the anterior chamber through the pupil or iridectomy. In these cases, the aqueous humor accumulates behind the iris, causing a forward shift of the iris and narrowing of the anterior chamber angle. This condition may be distinguished from the much less common malignant glaucoma in aphakia by the deeper central anterior chamber and forward bowing of the peripheral iris in the eyes with aphakic pupillary block glaucoma.

In Pseudophakia

Pupillary block glaucoma in pseudophakia was once seen most often with anterior chamber and iris-supported lenses, With anterior chamber lenses, the iris bulges forward on either side of the lens, whereas the mechanism with posterior chamber lenses appears to be excessive inflammation with posterior synechiae to the intraocular lens or the anterior lens capsule[6]

Peripheral Anterior Synechiae or Trabecular Damage

In most cases of chronic glaucoma in aphakia or pseudophakia, peripheral anterior synechiae are present, presumably because of a flat anterior chamber or the presence of inflammation or debris in the early postoperative period. Flat anterior chambers after cataract surgery may be caused by a wound leak with subsequent hypotony and choroidal detachments. The mechanism of aqueous outflow obstruction in cases of chronic open-angle glaucoma (COAG) in aphakia or pseudophakia is most likely related to alterations in the trabecular meshwork due to the surgery and possibly a preexisting reduction in outflow facility. In many of these patients, COAG may have been present but undiagnosed preoperatively.[6]

Distortion of the Anterior Chamber Angle

Campbell and Grant provided evidence that distortion of the anterior chamber angle is induced by tight corneoscleral sutures, whereas Kirsch and colleagues suggested that edema of the deep corneal stroma is the mechanism. Whatever the initiating factors may be, the internal white ridge in corneoscleral incision described by Krisch et al is known to be associated with the formation of peripheral anterior synechiae, vitreous adhesions, and hyphema. In some cases, it is likely that the white ridge contributes to the early, transient pressure elevation after cataract surgery.[6]

Chymotrypsin Glaucoma

Chymotrypsin-associated IOP elevation is seen quite rarely today because intracapsular cataract extraction with chymotrypsin is rarely performed. The generally accepted mechanism for chymotrypsin glaucoma is that zonular fragments obstruct the outflow channels.[5]

Nd:YAG Laser Posterior Capsulotomy

The mechanism of IOP elevation after Nd:YAG capsulotomy is not fully understood, Most cases have an open-angle mechanism, and the obstruction of the trabecular meshwork may be with fibrin and inflammatory cells due to a breakdown in the blood-aqueous barrier or debris from the capsule or cortical remnants . Other reported mechanisms of IOP elevation include pupillary block due to forward movement of the vitreous and herniated vitreous occluding a pre-existing glaucoma surgical fistula.[6]

Aqueous Misdirection Syndrome

First described by von Graefe in 1869, malignant glaucoma denotes a process involving a shallow central AC associated with increased IOP. Although typically occurring early in the postoperative period, it can be delayed by weeks or years. Mechanisms like apposition of the ciliary process against the lens or vitreous, posterior diversion of aqueous, and iris abutting against the AC angle by forward displacement of the lens have been proposed. A small middle segment, sudden hypotony, inflammation, hyaloid abnormality, sudden blockage of posterior to anterior flow of aqueous may initiate it.[2]


Some of the ways to evaluate the patient presenting with glaucoma include utilizing gonioscopy, optical coherence tomography, ultrasound biomicroscopy (UBM) and Scheimpflug video imaging [7],[8].UBM provides non-invasive, high-definition, reliable, and repeatable, cross-sectional images of the iris, posterior chamber IOL, lens zonule, ciliary body and even the anterior choroid [9]. UBM provides measurements of several angle parameters, including the trabecular-iris angle, the trabecular-ciliary process distance, iris thickness, iris-ciliary process distance, iris-IOL contact distance, iris-zonular distance, AC angle, iris-IOL angle, and AC depth [10]. UBM can be used to detect causes of pseudophakic glaucoma such as malposition of the IOL,[11] pupillary block glaucoma,[12] misplaced haptics, anterior and posterior synechiae, as well as occlusion of the trabecular meshwork by inflammatory cells and debris.[13]


Preoperative Considerations

Pressure Reduction

Many surgeons elect to reduce the vitreous volume and IOP by applying external pressure to the globe before surgery to maintain a deep anterior chamber and to minimize the potential complications of vitreous loss and expulsive hemorrhage. The external force may be accomplished by digital pressure, a rubber ball with an elastic band around the head, or a pneumatic rubber balloon (i.e., a Honan IOP reducer).

Use of these approaches may be unnecessary if topical or subconjunctival anesthesia is used.[6] Intravenous hyperosmotic agents such as mannitol can be utilized to reduce the risk of complications.[3]

Selection of Intraocular Lens

Intraocular lens implantation in the posterior chamber in association with extracapsular cataract extraction and phacoemulsification is generally associated with a slight reduction in postoperative IOP and is well tolerated even in eyes with advanced pre-existing glaucoma where IOP is satisfactorily controlled. Anterior chamber lenses, however, are more problematic, and preoperative glaucoma or anterior chamber angle abnormalities are relative contraindications to their use.[6]

Intraoperative Considerations

Attention to gentle handling of tissues, hemostasis, and minimal intraocular manipulation may reduce the risk of postoperative IOP rise associated with hemorrhage or excessive inflammation or pigment dispersion. One study found that the technique of wound closure (specifically, a sutureless sclerocorneal tunnel incision), Judicious use of intraocular agents such as viscoelastic substances and thorough irrigation to remove the material at the end of the case, especially in eyes with preexisting glaucoma, may help to minimize the risk of postoperative glaucoma complications.[6]

Intraoperative use of miotic agents, acetylcholine and carbachol provides pressure reduction in addition to constriction of the pupil (miosis) up to 24 hours after surgery.

Early Postoperative Period

The IOP can rise a few hours after routine cataract extraction but generally returns to normal within 1 to 3 days.[6] If there is pain or a threat to the optic nerve head, cornea, or cataract incision, temporary medical measures should be used such as carbonic anhydrase inhibitors, prostaglandin analogs, beta-blockers, alpha2-antagonists or oral acetazolamide. Use of prostaglandin analogs in early post-operative period varies among practitioners due to their inflammatory properties.[3]

If IOP is causing significant corneal edema, discomfort, and there is pre-existing glaucoma, anterior chamber tap could be done successfully at the slit lamp by releasing aqueous through existing paracentesis from cataract surgery. Prior to paracentesis, the eye should be prepped with 5% betadine or antibiotic. The aim should be to lower the IOP to high 10s or low 20s rather then returning IOP to single digits.[3]

When uveitis and glaucoma are associated with retained lens fragments in the vitreous, pars plana vitrectomy is reported to yield good results [6]. Uveitis, glaucoma, and hyphema may be managed by using mydriatic agents to minimize iris movement against the lens in mild cases. In more severe cases, steroids should be used for the iritis, and a carbonic anhydrase inhibitor or topical ß-blocker or a2-agonist for the glaucoma. Argon laser photocoagulation may be effective in controlling the haemorrhage in the rare cases in which the bleeding site is visible . Recurrent hyphema and glaucoma is usually an indication to remove the lens implant, although this is often difficult and can lead to serious intraoperative complications. When glaucoma and hyphema are associated with vitreous haemorrhage, pars plana vitrectomy has been recommended [6].

Pigment dispersion in pseudophakia can usually be controlled medically and gradually becomes easier to manage in most cases; removal of the lens implant is rarely required. Pupillary block in aphakia may initially be treated with mydriasis to break the block, although an iridotomy is usually required. Suggested alternative surgical approaches include separating the iris from the vitreous adhesions with laser iridoplasty, an iris repositor, or pars plana vitrectomy. Pupillary block in pseudophakia may be broken with mydriatic therapy by enlarging the pupil beyond the edges of an anterior chamber lens or by lysing posterior synechiae from a posterior chamber lens. Iridotomy is also required. Closed vitrectomy has also been used to relieve pseudophakic pupillary block .

In pupillary block use of one or more of the following agents may also be required as an emergency measure carbonic anhydrase inhibitor, hyperosmotic agent, ß-blocker, a2-agonist [6]. For Malignant Glaucoma medical therapy may be curative and includes

aqueous suppression, cycloplegia, and hyperosmotic agents. Hyperosmotics decrease the pressure exerted by the vitreous, whereas cycloplegics pull the lens back by tightening the zonules. If the condition persists, YAG capsulotomy and anterior hyaloidotomy to disrupt the anterior hyaloid face and the posterior capsule may be needed. Vitrectomy with anterior chamber deepening may be required.[2]

Late Postoperative Period

Most patients with chronic glaucoma in aphakia or pseudophakia can and should be managed medically. Surgical intervention is reserved for cases that are uncontrolled on maximum tolerable medical therapy. Laser trabeculoplasty may be effective in cases that do not have extensive peripheral anterior synechiae and is the initial surgical procedure of choice. When conjunctival scarring does not allow performance of a trabeculectomy in a superior quadrant, implantation of a glaucoma drainage device is usually indicated.[6]

Diode cyclophotocoagulation may be spared for those with advanced disease with poor vision [3]. When Nd:YAG capsulotomy is required in the late postoperative period, apraclonidine (1.0% or 0.5%), timolol, or acetazolamide given 1 hour before or immediately after the procedure, or both, effectively minimizes the post laser pressure rise [6]

In conclusion, glaucoma in pseudophakia and aphakia is common and early diagnosis and treatment could provide the best outcome.


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Dr. Aishwarya R. Mulay
Cataract and Glaucoma Consultant, Mulay Eye Clinic, Pune, Maharashtra
Dr. Aishwarya R. Mulay completed her MBBS from Smt. Kashibai Navale Medical College and General Hospital, Pune. She completed her postgraduation from National Institute Of Ophthalmology (NIO), Pune , followed by long term Cataract and Phaco Fellowship from K. B. Haji Bachooali Charitable Ophthalmic & ENT Hospital, Mumbai. She underwent medical and surgical training in Glaucoma From PBMAs H. V. Desai Eye Hospital, Pune. Currently she is working as Cataract and Glaucoma Consultant at Mulay Eye Clinic, Pune and also working with KEM Hospital Pune, Sahyadri Hospital Pune, Dr. Agarwals Eye Hospital Pune, Dada laser eye institute.
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